Relevant to our studies and the shared capacity of BACE2 to proteolytically cleave IAPP and Aβ, Jackson et al described identifying IAPP deposition in the temporal lobe gray matter, blood vessels and perivascular spaces of T2D patients and found mixed IAPP-Aβ deposits in the blood vessels and brain parenchyma of late onset AD patients [52]. This evidence concerns the gene BACE2 and Alzheimer disease.